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Am J Physiol Endocrinol Metab (July 30, 2002). doi:10.1152/ajpendo.00436.2001
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Articles in PresS, published online ahead of print July 30, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00436.2001
Submitted on September 27, 2001
Accepted on July 11, 2002

Effect of Endotoxin on Expression of TNF receptors and Transport of TNF{alpha} at the Blood-Brain Barrier of the Rat

Berit Osburg1, Christian Peiser2, Dietmar Domling3, Lutz Schomburg4, Young-Tak Ko5, Karlheinz Voigt3, and Ulrich Bickel5*

1 Department of Pharmaceutical Sciences, Texas Tech University Health Sciences Center, School of Pharmacy, Amarillo, Texas, USA; Institute of Physiology, Philipps-University, Marburg, Germany
2 Departments of Pediatric Pneumology and Immunology, Humboldt University, Charite, Berlin, Germany
3 Institute of Physiology, Philipps-University, Marburg, Germany
4 Neuroscience Research Center, Humboldt University, Charite, Berlin, Germany
5 Department of Pharmaceutical Sciences, Texas Tech University Health Sciences Center, School of Pharmacy, Amarillo, Texas, USA

* To whom correspondence should be addressed. E-mail: ubickel{at}ama.ttuhsc.edu.

The transport mechanism mediating brain uptake of tumor necrosis factor (TNF{alpha}) has been studied. When 125I-labeled rat TNF{alpha} was used in internal carotid artery perfusions in rats, the cytokine showed transcytosis through the blood-brain barrier in intact form (permeability-surface area product 0.34 ± 0.13 µL min-1 g-1). Uptake was inhibited by low nanomolar concentrations of unlabeled rat TNF{alpha}. Human TNF{alpha}, which does not interact with the p80 TNF receptor in rodents, showed no brain uptake. mRNA expression of both p60 and p80 receptors could be demonstrated in native brain microvessel preparations. These transcripts increased to 149% of control (p60), and 127% (p80) 4 h after a systemic immune stimulation (2 mg/kg bacterial endotoxin, intraperitoneal). Lipopolysaccharide treatment did not alter the rate of brain uptake of TNF[{alpha} measured between 4 and 24 h later. In conclusion, a receptor-mediated mechanism is responsible for the transcytosis of TNF{alpha}. Saturable transport, requiring the p80 receptor, occurs at concentrations encountered under pathophysiological conditions, and therefore constitutes a relevant mechanism of communication between the immune system and the brain.




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